Endocrine System 3: Thyroid And Parathyroid Glands
Copyright EMAP Publishing 2021This article is not for distributionexcept for journal club useClinical PracticeSystems of lifeEndocrine systemKeywords Thyroid/Parathyroid/Endocrine system/HormonesThis article has beendouble-blind peer reviewedIn this article. H ow thyroid hormones T3 and T4 act to regulate cellular metabolism Clinical features of hypothyroidism and hyperthyroidism The role of the thyroid and parathyroid glands in maintaining calcium homeostasisEndocrine system 3:thyroid and parathyroid glandsKey pointsThe thyroid is in theneck, just below theAdam’s apple, andcontains four tiny,independentlyfunctioning,parathyroid glandsThyroid follicularcells secreteiodine-richhormones, T3 andT4, which helpregulate metabolismRelease of T3 andT4 is modulated byhypothalamus andpituitary glandhormonesHypothyroidism andhyperthyroidism arecommon thyroiddisorders, oftentreatable with drugsor radioactive iodinetherapyCalcitonin producedby the thyroid worksantagonistically withparathyroidhormone to maintaincalcium homeostasisAuthors John Knight is associate professor in biomedical science; Maria Andrade ishonorary associate professor in biomedical science; Zubeyde Bayram-Weston issenior lecturer in biomedical science; all at College of Human and Health Sciences,Swansea University.Abstract The endocrine system comprises glands and tissues that produce hormonesto regulate and coordinate vital bodily functions. This article, the third in an eight-partseries on the endocrine system, examines the anatomy and physiology of the thyroidand parathyroid glands, and the pathophysiology associated with some commonthyroid diseases.Citation Knight J et al (2021) Endocrine system 3: thyroid and parathyroid glands.Nursing Times [online]; 117: 7, 46-50.This eight-part series on the endocrine system opened with anoverview of endocrine glands andthe role of hormones as chemicalsignals that help maintain the homeostaticbalance that is essential to health; theremaining articles each explore differentmajor endocrine glands and tissues. Thesecond article in the series focused on thehypothalamus and pituitary gland. In thisthird article, we explore the anatomy andphysiology of the thyroid and parathyroidglands, as well as the pathophysiology ofsome common thyroid diseases.Thyroid glandAnatomyThe thyroid is a bi-lobed gland, oftendescribed as resembling a butterfly or bowtie. It is positioned in the neck, between theC5 and T1 vertebrae, just below the thyroidcartilage (Adam’s apple) of the larynx. Itconsists of two major lobes (right and left),which are connected by a smaller piece oftissue called the isthmus; around half ofindividuals also possess an additional thirdlobe, usually triangular shaped and knownas the pyramidal lobe (Fig 1). The weight ofNursing Times [online] July 2021 / Vol 117 Issue 7 46the adult thyroid gland varies between 15gand 30g, and each of the major lobes isaround 4cm long and 2cm wide (Benvengaet al, 2018; Dorion, 2017). Embedded in theposterior portion of the thyroid are fourtiny parathyroid glands, which functionindependently of the thyroid (Fig 1).HistologyThe thyroid contains two major populations of endocrine cells: F ollicular cells – each major lobe of thethyroid consists of smaller lobules thatare composed of sac-like follicles (Fig 2).The walls of each follicle primarilyconsist of cube-shaped cells. Thesesynthesise and secrete iodine-richhormones that regulate metabolism; P arafollicular cells – these are found inmuch smaller numbers, interspersedbetween the thyroid follicles, andsynthesise calcitonin, a hormone thathelps maintain calcium homeostasis.Thyroid hormones: T3 and T4The follicular cells of the thyroid producetwo iodine-containing hormones, calledT3 and T4 (also known as thyroxine). Eachwww.nursingtimes.net
Copyright EMAP Publishing 2021This article is not for distributionexcept for journal club useClinical PracticeSystems of lifeFig 1. Thyroid and parathyroid glandsFig 2. Follicular and parafolicular cells of the thyroid glandJENNIFER N.R. SMITHFig 3. Structure of tyrosine, T3 and T4molecule of T3 (triiodothyronine) hasthree atoms of iodine, while each moleculeof T4 (tetraiodothyronine) has four iodineatoms. To ensure normal biosynthesis ofT3 and T4, it is essential to maintain anadequate intake of iodine in the diet.Seafood, including most types of fishand shellfish, are particularly rich sourcesof this trace mineral. Smaller amounts arealso found in eggs, red meats, poultry anddairy products, including, milk, yoghurtand cheeses. For vegetarians and vegans,various forms of kelp (seaweed) offer anincredibly rich source of iodine, withNursing Times [online] July 2021 / Vol 117 Issue 7 47smaller amounts present in potato skins,watercress, kale, green beans, cranberries,strawberries and most types of nut. Manypeople supplement their iodine intakewith combined multivitamin and mineralpreparations or iodised table salt. The current recommended daily intake (referenceintake) of iodine for adults is 140-150µg,rising to 200µg in women who are pregnant or breastfeeding (Bit.ly/NHSIodine;Bit.ly/BDAIodine).Around 90% of dietary iodine is rapidlyabsorbed in the stomach and duodenumbefore circulating in the blood (Leung et al,2010). The majority of plasma iodine istaken up by the thyroid gland and anyexcess is eliminated efficiently by the kidneys. The follicular cells of the thyroid areequipped with transporter proteins in theircell membranes; these facilitate rapiduptake of iodine, which is then joined to alarge protein called thyroglobulin. Thisiodised thyroglobulin is stored and concentrated in the centre of the thyroid follicles, where it forms the major componentof a homogenous suspension called colloid(Fig 2).Thyroglobulin is rich in the amino acidtyrosine, which provides the substrate forthe biosynthesis of thyroid hormones T3and T4. These thyroid hormones are composed of two molecules of tyrosine linkedtogether, containing three (T3) or four (T4)atoms of iodine (Fig 3). When T3 and T4 arerequired, small droplets of iodised thyroglobulin are taken back into the follicularcells from the central colloid. The thyroglobulin is digested by intracellular enzymes torelease individual molecules of T3 and T4(Benvenga et al, 2018; Leung et al, 2010).Like all endocrine glands, the thyroid ishighly vascularised and T3 and T4 arereleased directly into the blood. Proportionally, the thyroid gland releases approximately 80% T4 and 20% T3, although it isestimated that T3 has around four timesthe potency of T4 (Sargis, 2019). Both hormones have very low solubility in theaqueous environment of the plasma so aretransported around the body bound toplasma proteins. These include:l A lbumin (the most abundant plasmaprotein);l T ransthyretin;l T hyroxine-binding globulin (TBG).Each of these three plasma proteins issynthesised by the liver, with TBG havingthe highest binding affinity (Chakravarthyand Ejaz, 2020). T3 and T4 are bound totheir plasma protein vehicles but cannotexert any biological effects; however, smallamounts of T3 and T4 detach and, oncewww.nursingtimes.net
Copyright EMAP Publishing 2021This article is not for distributionexcept for journal club useClinical PracticeSystems of lifefree, are able to exert their effects.Free T3 and T4 cross into their targetcells and bind to thyroid hormone receptors (THRs) located in the cell nucleus.Both hormones can bind to THRs, but T3binds with a much greater affinity than T4.Many of the target cells have enzymes,called deiodinases, which rapidly removean atom of iodine from the T4 molecules,thereby generating greater amounts of themore-potent T3 (Shahid et al, 2020).Biological effects of T3 and T4Virtually all human cells and tissues haveTHRs and can respond to free T3 and T4,which play an essential role in regulatingcellular metabolism.To release the energy needed to drive thebiochemical processes necessary to sustainlife, cells need to use simple food-derivedmolecules, such as sugars and fats. The primary – and preferred – energy source formost human cells is glucose, a monosaccharide sugar. In cells, glucose is metabolised inthe cytoplasm using specialised organellescalled mitochondria. These contain respiratory enzymes, which progressively releaseenergy from the chemical bonds present inglucose molecules, and use this to synthesise the energy storage molecule, adenosinetriphosphate (ATP). This process occursmost efficiently in the presence of oxygen(aerobic cellular respiration), with eachmolecule of glucose (under normal conditions) typically yielding around 29-32 molecules of ATP (Flurkey, 2010).As a by-product of cellular metabolism,heat is also generated; this is dissipatedthrough the body via circulating blood andother bodily fluids. This heat generation iscalled thermogenesis and is vital to helpmaintain the body’s core temperature ataround 370C, the optimal temperature forthe functioning of most human enzymes.The rate at which food-derived molecules, such as fats, proteins and glucose,are metabolised to release energy is largelygoverned by T3 and T4 levels. In addition toregulating metabolism, T3 and T4 alsoinfluence a variety of other physiologicalprocesses, including heart and respiratoryfunction, muscle strength, neural function and the level of cholesterol in theblood (Sargis 2019, VanPutte et al 2017).The hypothalamus continually monitorsthe concentration of T3 and T4 circulatingin the plasma. When levels of T3 and T4decrease, the hypothalamus synthesisesand releases thyrotropin-releasing hormone (TRH). TRH is a small peptide thatbinds to receptors in the anterior pituitary,initiating the secretion of thyroid stimulating hormone (TSH). TSH (another peptide hormone) circulates in the blood beforebinding to its complementary receptors onthe follicular cells of the thyroid gland,which then release T3 and T4 (Fig 4).The HPT axis is fine-tuned via continualnegative feedback. Increased levels of T3and T4 circulating in the plasma aredetected by the hypothalamus, reducingthe secretion of TRH. This reduces therelease of TSH by the anterior pituitarygland, thereby reducing the release of T3and T4 secretion (Chiasera, 2013). Tighthomeostatic regulation of the HPT axisusually ensures a relatively stable metabolic rate but thyroid disorders, which canupset homeostasis are common; these areexplored below.HypothyroidismHypothyroidism is the term for an underactive thyroid gland and is characterisedby a deficiency in levels of circulating T3and T4. Hypothyroidism is the mostcommon thyroid disorder; UK incidence isaround 2%, increasing to 5% in people 60 years, with women five to 10 timesmore likely to be affected compared withmen (National Institute for Health andCare Excellence (NICE), 2019).The most common form of hypothyroidism is primary hypothyroidism. Inareas where the diet is not deficient iniodine, the major form of primary hypothyroidism is an autoimmune disease calledHashimoto’s thyroiditis (Chaker et al, 2017).The precise cause of this disease remainsunclear, but it is associated with theproduction of autoantibodies that bind tothe follicular components of the thyroidgland, which are progressively destroyed bythe patient’s own immune system. The condition is associated with varying degrees ofinflammation of the thyroid, while loss offollicular cells results in reduced secretionof T3 and T4, and a reduced metabolic rate(Machala et al, 2019).Blood tests usually reveal significantlyelevated levels of TSH in patients withHashimoto’s thyroiditis (Chaker et al,2017). This is because the low circulatinglevels of T3 and T4 are detected by thehypothalamus, which releases TRH, initiating the release of TSH from the anteriorpituitary. Ageing is often linked to anincrease in circulating autoantibodies thatreact with the follicular cells of the thyroidgland (Calsolaro et al, 2019); this may partially explain the reduction in basal metabolic rate usually observed in old age.Although the recommended dailyintake for iodine is low, many people aredeficient in the mineral. In some parts ofthe UK, and more often in landlockedregions of Africa and Asia, access toiodine-rich marine food sources is limited.This can result in chronic iodine deficiency, which may cause hypothyroidism.Prolonged iodine deficiency is oftenassociated with a pronounced swelling ofthe thyroid gland, known as a goitre; thiscan be disfiguring and visibly stretch theskin at the front of the neck. Worryingly,despite initiatives to improve iodineintake, iodine deficiency is thought toaffect around 2 billion of the world’s population (Li and Eastman, 2012).Insufficient iodine intake during pregnancy can lead to congenital iodine deficiency syndrome (also known as cretinism). Iodine is essential for the centralnervous system to develop normally, anddeficiency is associated with varyingdegrees of brain damage. This can result inFig 4. Hypothalamic-pituitary-thyroid axisHypothalamic-pituitary-thyroid axisThe release of T3 and T4 by the thyroid ismodulated by hormones produced by thehypothalamus and pituitary gland; thisregulatory mechanism is referred to asthe hypothalamic-pituitary-thyroid axis(HPT axis).Nursing Times [online] July 2021 / Vol 117 Issue 7 HypothalamusThyrotropin-releasing hormone (TRH)PituitaryThyroid stimulating hormone (TSH)NegativefeedbackThyroidThyroid hormone T4Thyroid hormone T3Increased metabolism48www.nursingtimes.net
Copyright EMAP Publishing 2021This article is not for distributionexcept for journal club useClinical PracticeSystems of lifeTable 1. Signs and symptoms of hypothyroidism and hyperthyroidismClinical reased, with tendency for weight gain;difficulty losing weight; decreased bodytemperature; cold intolerance; cold hands and feet;shivering; fatigue and lethargyIncreased, with tendency for weight loss; increasedbody temperature; heat intolerance; increasedappetiteCentral nervous systemDepression; poor memory; sluggish speech; slowreflexesOverstimulation; agitation; poor concentration;anxiety; insomnia; nervous tics; mood swings; tremorsIntegumentary systemDry, scaly skin; decreased sweating, thickeneddystrophic nails, coarse hair, hair loss on scalp andeyelids, puffy faceIncreased sweating; thinning skin; flushed skin; fine,brittle hair; thin, soft nails; itchiness and skin rashesCardiovascular systemReduced heart rate, increased cholesterolTachycardia; arrhythmias; systolic hypertensionReproductive systemReduced fertility, decreased libido, heavy andprolonged periods, miscarriageIrregular/light periods; amenorrheaMiscellaneousConstipation, goitre, muscle cramps, hoarse voice,joint painIncreased bowel movements; nausea; exophthalmos(bulging eyes)impaired neurocognitive development,speech and hearing deficits, and muscularand gait problems. Many affected individuals may also display: impaired growth;dry, thickened skin; poor/sparse hairgrowth; and gastrointestinal problems(Toloza et al, 2020).Secondary and tertiary hypothyroidismOccasionally, reduced levels of T3 and T4are found when the thyroid gland ishealthy and receiving a steady supply ofiodine. This can occur due to abnormalities affecting the anterior pituitary gland,such as tumours, which reduce the synthesis and release of TSH. Without adequate TSH stimulation, the follicular cellsof the thyroid gland release less T3 and T4,and metabolic rate falls; this is referred toas secondary hypothyroidism (BeckPeccoz et al, 2017).Even more rarely, damage to the hypothalamus, potentially due to head trauma orsurgery, may reduce or stop the release ofTRH. This will prevent the release of TSHfrom the anterior pituitary and lead toreductions in T3 and T4; this is known astertiary hypothyroidism (Chaker et al, 2017).Clinical features of hypothyroidismUnsurprisingly, a reduced metabolic ratemeans people with hypothyroidism oftengain significant weight. As less energy isbeing released from food, with no decreasein food intake there is a calorific surplusand increased fat deposition. Patients withhypothyroidism also generate substantially less heat through thermogenesis andoften complain of feeling cold all the time;other common symptoms of hypothyroidism are highlighted in Table 1.Unintended weight gain and a reducedcore temperature are the classic symptomsof hypothyroidism, and necessitate a fullthyroid function evaluation. Fortunately,treatment for the most common forms ofhypothyroidism is usually fairly straightforward and relies on taking levothyroxine. This drug is a synthetic form of T4and is usually taken once a day in tabletform (Bit.ly/NHSLevothyroxine). For adultpatients beginning levothyroxine treatment, it is advisable to monitor the level ofTSH every three months until it has stabilised to within the normal reference range,and then once yearly (NICE, 2019).HyperthyroidismHyperthyroidism is the term for an overactive thyroid, with consistently elevatedsecretion of T3 and T4. The most commonform of hyperthyroidism is an autoimmune disorder called Graves’ disease; inthe UK this affects around 2% of womenand 0.2% of men (NICE, 2019).Graves’ disease is characterised by theproduction of autoantibodies that bind tothe same receptors as TSH. These autoantibodies act as TSH mimics, increasing therelease of T3 and T4 beyond their normalphysiological concentrations. Althoughthe exact causes are poorly understood, themajor risk factors are being female (true formost autoimmune diseases) and a familyhistory of autoimmune disease (Campi andSalvi, 2018). The disease can usually be confirmed by the detection of TSH-receptorautoantibodies in the plasma.Clinical features of hyperthyroidismIn many ways, the primary symptoms ofhyperthyroidism are the opposite ofNursing Times [online] July 2021 / Vol 117 Issue 7 49hypothyroidism: an increased secretion ofT3 and T4 raises the metabolic rate, whichoften results in marked weight loss. Asfood molecules are metabolised more rapidly, there is greater thermogenesis, raisingthe body’s core temperature and leading toheat intolerance and increased sweating.Other common clinical features of hyperthyroidism are summarised in Table 1.One of the most dramatic clinical features of Graves’ disease is an accumulationof inflamed, fibrous, fatty tissue behindthe eyes, which can cause a prominentbulging of the eyes, called exophthalmus.In severe cases, this may result in progressive eyelid retraction and compressiveoptic neuropathy, which may affect vision.This collection of clinical featuresaffecting the eyes is known as Graves’ ophthalmopathy and affects around 50% ofpeople with the disease to varying degrees(Al-Sharif and Alsuhaibani, 2017). The perceived disfigurement caused by pronounced exophthalmos can cause emotional distress and impaired psychosocialhealth. This has led to various surgicalinterventions aimed at removing excesstissue behind the eye (orbital decompression), which are largely shown to be safeand effective at improving cosmetic appearance (Al-Sharif and Alsuhaibani, 2017).Transient or mild hyperthyroidism canbe treated using the drug carbimazole,which inhibits the addition of iodine totyrosine residues in the thyroid, therebyreducing the release of T3 and T4. However,in most adults with hyperthyroidism, radioactive iodine (radioiodine) therapy is recommended as a first-line treatment; thisprovides accurate and targeted therapy asthe follicular portions of the thyroid glandwww.nursingtimes.net
Copyright EMAP Publishing 2021This article is not for distributionexcept for journal club useClinical PracticeSystems of lifeare so effective at taking up and concentrating iodine. I-131 is an isotope that emitsgamma radiation; this damages and killsthe follicular cells, leading to a significantreduction in the secretion of T3 and T4.Radioiodine therapy is not used in womenwho are pregnant or breastfeeding or inmale or female patients planning for apregnancy in the next 4-6 months.Surgical removal of the thyroid (thyrodectomy) is recommended when thyroidmalignancy is suspected or there is significant enlargement of the thyroid tissues andrisk of tissue compression. Following radioiodine therapy or thyroidectomy, secretion of T3 and T4 declines, and manypatients will develop hypothyroidism. Thisusually requires levothyroxine therapy,often for the rest of the patient’s life (BritishThyroid Association, 2019; NICE, 2019).Calcium homeostasisCalcium plays many diverse roles inhuman physiology including: M aintenance of bone density and toothhealth; T riggering of muscle contraction; Cell division; Secretion from glands; S ynaptic transmission of nerveimpulses; A cting as a cofactor for multipleenzymes; Haemostasis and blood coagulation.It is essential that calcium is alwaysfreely available and is dissolved in theblood and other bodily fluids at the correctconcentration. It is the most tightly regulated of all the major plasma electrolytes,having an incredibly narrow normal rangeof 2.1-2.6mmol/l (Bazydlo and Needham,2014). This is achieved primarily throughthe actions of two antagonistic hormones: C alcitonin, produced by the thyroid; P arathyroid hormone (PTH), producedby the parathyroid glands.Parafollicular cells and calcitoninThe parafollicular cells (also known asC-cells) are scattered between the folliclesof the thyroid gland in relatively smallnumbers and make up only around 0.1% ofthe total thyroid cells (Benvenga et al,2018). Although the parafollicular cells arean intrinsic part of the thyroid gland, theiractivity is not regulated by the HPT axis;instead, they act independently, continually monitoring plasma–calcium concentration. When plasma calcium rises (forexample, after eating calcium-rich dairyfood, such as cheese) these cells release thepeptide hormone calcitonin. The majoreffect of calcitonin is to reduce theplasma–calcium concentration; this isachieved by two main mechanisms: I nhibition of osteoclast activity – boneis a dynamic tissue continually built upby cells called osteoblasts (boneforming cells) and broken down by cellscalled osteoclasts (VanPutte et al, 2017).These two groups of cells usually workat similar rates to maintain bonedensity. The skeleton acts as a calciumreservoir, storing around 99% of thetotal calcium present in the body. Byinhibiting the activity of osteoclasts,calcitonin allows the bone-formingosteoblasts to freely deposit the excesscalcium in the bones, normalisingplasma–calcium concentration; D ecreasing tubular re-absorption ofcalcium by the kidneys – calcitonininhibits re-absorption of calcium fromthe renal filtrate into the blood. Thisallows excess calcium to be rapidlyeliminated in the urine, reducing theplasma–calcium concentration(Summers and Macnab, 2017).Parathyroid glandsThe parathyroid glands are found in theposterior portion of the thyroid gland(Fig 1). There are usually four, each 3-5mmin diameter, which tend to be oval-to-roundin shape and weigh around 35mg (Benvengaet al, 2018; Dorion, 2017). Each parathyroidgland contains a population of cells calledchief cells, which synthesise parathyroidhormone (PTH or parathormone).PTH is a small peptide hormone thatprimarily works antagonistically to calcitonin to help maintain calcium homeostasis. The chief cells monitor plasma–calcium concentration and release PTH whenplasma–calcium levels decrease. PTHenhances osteoclast activity, increasing thebreakdown of bone and the release of calcium and phosphate (the two major inorganic mineral components of bone) intothe plasma. This begins to increase andnormalise the plasma–calcium concentration. As well as stimulating calcium releasefrom the skeletal reservoir, PTH furtherincreases plasma–calcium by enhancingtubular calcium re-absorption in the kidneys (Summers and Macnab, 2017).ConclusionThis article has examined the anatomy andphysiology of the thyroid and parathyroidglands, and outlined hypothyroidism andhyperthyroidism. Part 4 of this series willexplore the adrenal glands and the diverseroles they play in human physiology. NTNursing Times [online] July 2021 / Vol 117 Issue 7 50ReferencesAl-Sharif E, Alsuhaibani AH (2017) Fat-removalorbital decompression for thyroid associatedorbitopathy: the right procedure for the right patient.Saudi Journal of Ophthalmology; 31: 3, 156–161.Bazydlo LAL, Needham M (2014) Calcium,magnesium, and phosphate. Laboratory Medicine;45: 1, e44–e50.Beck-Peccoz P et al (2017) Centralhypothyroidism: a neglected thyroid disorder.Nature Reviews: Endocrinology; 13: 10, 588–598.Benvenga S (2018) Thyroid gland: anatomy andphysiology. Encyclopedia of Endocrine Diseases; 4,382-390.British Thyroid Foundation (2019) Your Guide toTreatment of an Overactive or Enlarged ThyroidGland with Radioactive Iodine. BTFCalsolaro V et al (2019) Overt and subclinicalhypothyroidism in the elderly: when to treat?Frontiers in Endocrinology; 10: 177.Campi I, Salvi M (2018) Graves’ disease.Encyclopedia of Endocrine Diseases; 4, 698-701.Chaker L et al (2017) Hypothyroidism. Lancet; 390:10101, 1550–1562.Chakravarthy V, Ejaz S (2020) Thyroxine-bindingglobulin deficiency. In: StatPearls [internet].StatPearls Publishing.Chiasera JM (2013) Back to the basics: thyroidgland structure, function and pathology. AmericanSociety for Clinical Laboratory Science; 26: 2, 112-117.Dorion D (2017) Thyroid anatomy. medscape.com,30 November 2017.Flurkey WH (2010) Yield of ATP molecules perglucose molecule. Journal of Chemical Education;87: 3, 271.Leung A et al (2010) Role of iodine in thyroidphysiology. Expert Review of Endocrinology andMetabolism; 5: 4, 593–602.Li M, Eastman CJ (2012) The changingepidemiology of iodine deficiency. Nature Reviews:Endocrinology; 8: 7, 434-440.Machala E et al (2019) Hashimoto’s thyroiditis.World Scientific News; 128: 2, 302-314.National Institute for Health and Care Excellence(2019) Thyroid Disease: Assessment andManagement. NICE.Sargis RM (2019) How your thyroid works:controlling hormones essential to your Metabolism.endocrineweb.com, 21 October.Shahid MA et al (2020) Physiology, ThyroidHormone. In: StatPearls [internet]. StatPearlsPublishing.Summers R and Macnab R (2017) Thyroid,parathyroid hormones and calcium homeostasis.Anaesthesia & Intensive Care Medicine; 18: 10,522-526.Toloza FJK et al (2020) Consequences of severeiodine deficiency in pregnancy: evidence inhumans. Frontiers in Endocrinology; 11: 409.VanPutte CL et al (2017) Seeley’s Anatomy andPhysiology. McGraw-Hill.CLINICALSERIESEndocrine systemPart 1: Overview of the endocrine systemand hormonesPart 2: Hypothalamus and pituitary glandPart 3: Thyroid and parathyroid glandsPart 4: Adrenal glandsPart 5: Pineal and thymus glandsPart 6: Pancreas, stomach, liver, smallintestinePart 7: Ovaries and testes, placenta(pregnancy)Part 8: Kidneys, heart and skinMayJunJulAugSepOctNovDecwww.nursingtimes.net
the adult thyroid gland varies between 15g and 30g, and each of the major lobes is around 4cm long and 2cm wide (Benvenga et al, 2018; Dorion, 2017). Embedded in the posterior portion of the thyroid are four tiny parathyroid glands, which function independently of the thyroid (Fig 1). Histology The thyroid contains two major popula-
Thyroid antibodies in hypothyroidism In most instances, it is not necessary or recommended to check thyroid antibodies Elevated levels of thyroid antibodies may indicate that a patient with normal TSH and normal free T4 is more predisposed to develop hypothyroidism Elevated levels of thyroid antibodies do not indicate –
Endocrine System Modified by M. Myers. 2 The Endocrine System. 3 . 15 Anterior pituitary gland 1. Human growth hormone (hGH) (Somatotropin) 2. Thyroid stimulating hormone (TSH) 3. . Chapter 20: Endocrine System Author: Preferred Customer Created Date: 2/12/2011 1:03:24 PM .
Endocrine System. Quiz Answer Key. 1. True. or false: The endocrine system tells your cells when it's time to do important things, like grow. 2. Which one of these is a gland in your body? a. brain b. heart c. thyroid 3. Glands in your endocrine system release this into your body: a. water. b. fruit juice c. hormones 4. True or
Thyroid & parathyroid glands By Dr. Mohamed fathi Assistant professor Of Anatomy 1. By the end of this lectures we must know *Anatomical position, shape ,weight and capsule of thyroid gland. *Relation of thyroid gland. . Histology
2 shows the position of the thyroid gland as well as right and left lobe for a human being. Measurement of the thyroid in-volves three measurements, which are the width, depth and length [7]. The normal thyroid gland is 2cm or less in width and depth and 4.5 – 5.5 cm in length. 2.2 Fig. 2. Position of thyroid gland. [20]File Size: 600KBPage Count: 8
In order to measure normal thyroid gland in Sudanese. 1.4 Specific objectives: -To measure thyroid gland volume (right lobe, left lobe) and isthmus. -To correlate size of thyroid gland with body characteristics (age, gender, height and weight). -To find dynamic equation to calculate measurement of thyroid using body characteristics.
of 1432 Japanese with normal thyroid function [i.e., normal range of free triiodothyronine (free T3) and free . [the first quartile, third quartile]. Normal range of measurements are ( ) Table 2 Thyroid-related hormone by anti-thyroid peroxidase antibody (TPO-Ab) Anti-thyroid peroxidase antibody (TPO-Ab) p Total No. of participants 1165 267
The American Revolution had both long-term origins and short-term causes. In this section, we will look broadly at some of the long-term political, intellectual, cultural, and economic developments in the eigh-teenth century that set the context for the crisis of the 1760s and 1770s. Between the Glorious Revolution of 1688 and the middle of the eigh- teenth century, Britain had largely failed .
